Key result
Classical post-PCI microvascular dysfunction is linked to ~84% higher risk of MACE.
Why the study?
The specific determinants and long-term prognostic implications of endogenous and classical coronary microvascular dysfunction endotypes immediately after PCI in chronic coronary syndrome remained under-investigated.
Does the classical or endogenous endotype of post-PCI coronary microvascular dysfunction increase the risk of major adverse cardiac events in patients with chronic coronary syndrome undergoing elective PCI?
Observational (n=591)
Does the classical or endogenous endotype of post-PCI coronary microvascular dysfunction increase the risk of major adverse cardiac events in patients with chronic coronary syndrome undergoing elective PCI?
In patients with chronic coronary syndrome undergoing elective PCI, only the classical endotype of post-PCI coronary microvascular dysfunction independently drives long-term major adverse cardiac events, highlighting the need for endotype-specific risk stratification.
Endotype differentiation may refine post-PCI MACE risk assessment in chronic coronary syndrome; leaves open whether targeting classical CMD improves outcomes.
Background Coronary microvascular dysfunction (CMD) immediate post-percutaneous coronary intervention (PCI) is a heterogeneous condition comprising distinct "endogenous" and "classical" endotypes1. However, the specific determinants and long-term prognostic implications of these endotypes in chronic coronary syndrome (CCS) remain under-investigated. Purpose This study sought to identify the predictors of post-PCI CMD endotypes and evaluate their respective impacts on clinical outcomes. Methods We retrospectively analyzed 591 patients with CCS undergoing elective PCI with post-PCI comprehensive microvascular assessment. Post-PCI CMD (coronary flow reserve [CFR] < 2.0) was subclassified into endogenous (resting 1/transit-time > 1.85) and classical (resting 1/transit-time < 1.85) endotypes. The 1.85 cutoff was derived from the 29.3rd percentile of resting 1/transit-time values, corresponding to the distribution of impaired CFR. The primary endpoint was major adverse cardiac events (MACE), a composite of all-cause death, heart failure, and nonfatal myocardial infarction. The secondary endpoint was vessel-oriented composite outcomes (VOCO), a composite of target vessel related cardiac death, target vascular myocardial infarction and target vascular revascularization. Results Post-PCI CMD was present in 29.3% of patients (endogenous: 17.1%; classical: 12.2%). The endogenous endotype was associated with advanced age, female sex, and higher comorbidity, whereas classical CMD was characterized by an elevated index of microcirculatory resistance (IMR). Pre-PCI microvascular resistance reserve (MRR) was a robust independent predictor of post-PCI CMD. Over a median 4.75-year follow-up, classical CMD was independently associated with a significantly higher risk of MACE (Hazard Ratio [HR]: 1.84; 95% CI: 1.04–3.24; P=0.035), whereas endogenous CMD was not. In contrast, VOCO was independent of CMD status but was significantly predicted by post-PCI fractional flow reserve (HR: 0.0014; P=0.027). Conclusions Post-PCI CMD in CCS is a phenotypic mosaic. While pre-PCI MRR effectively predicts overall post-PCI microvascular impairment, only the classical endotype serves as a driver of long-term patient-oriented adverse events. These findings underscore the necessity of endotype-specific risk stratification to refine post-PCI management strategies.
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Watanabe et al. (2026) conducted an observational in Chronic coronary syndrome undergoing elective percutaneous coronary intervention (n=591). Post-PCI classical coronary microvascular dysfunction (CFR < 2.0 and resting 1/transit-time < 1.85) vs. Endogenous CMD or no post-PCI CMD was evaluated on Major adverse cardiac events (MACE), a composite of all-cause death, heart failure, and nonfatal myocardial infarction (HR 1.84, 95% CI 1.04-3.24, p=0.035). Classical post-PCI coronary microvascular dysfunction independently increased the risk of MACE (HR 1.84; 95% CI 1.04-3.24; P=0.035), whereas endogenous CMD did not.
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